Diabetology & Metabolic Syndrome最新文献

Background: The association between vitamin D status and mortality risk among adults with cardiovascular-kidney-metabolic (CKM) syndrome stages 0-3 requires further elucidation. We investigated the relationship between serum 25-hydroxyvitamin D [25(OH)D] levels and all-cause and cause-specific mortality among United States adults diagnosed with CKM syndrome stages 0-3.

Methods: Data from 37,551 adults presenting with CKM syndrome stages 0-3 were examined using National Health and Nutrition Examination Survey records (2001-2018). Death outcomes were determined via National Death Index linkage through December 31, 2019. Cox proportional hazards modeling and two-piecewise Cox regression approaches were utilized to assess nonlinear relationships between serum 25(OH)D levels and mortality risk, incorporating stratified analyses for high-risk population identification.

Results: Throughout 337,921 person-years of observation, we documented 4,039 deaths from all causes, encompassing 1,078 cardiovascular disease (CVD)-related deaths. Following multivariable adjustment, reduced serum 25(OH)D levels demonstrated significant associations with elevated all-cause and CVD mortality risk through nonlinear patterns. L-shaped dose-response curves emerged, revealing mortality risk plateaus at 52.20 nmol/L for all-cause mortality and 53.90 nmol/L for CVD mortality. Individuals maintaining 25(OH)D levels above these threshold values exhibited 2% reduced all-cause mortality risk (hazard ratio [HR] 0.98, 95% confidence interval [CI] 0.97-0.99) and 2% decreased CVD mortality risk (HR 0.98, 95% CI 0.97-0.99) relative to participants below these cutoff points.

Conclusions: Nonlinear relationships between serum 25(OH)D levels and both all-cause and CVD mortality were demonstrated among United States adults with CKM syndrome stages 0-3. These findings warrant confirmation through randomized controlled trials.

Aims: To investigate the role and underlying mechanisms of miR-4687-5p in diabetic retinopathy (DR) development.

Methods: A total of 180 DR patients were enrolled and stratified into non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR) groups. Concurrently, 100 type 2 diabetes mellitus (T2DM) patients and 100 healthy volunteers were recruited as control groups. DR cellular models were established by treating ARPE-19 cells with high glucose (HG). Reverse transcription quantitative polymerase chain reaction was used to detect gene expression. An in vitro DR cell model was constructed to explore the potential mechanism of miR-4867-5p in DR.

Results: Serum miR-4687-5p expression was significantly elevated in DR patients compared to healthy controls and T2DM patients, with the highest levels observed in PDR patients. This miRNA exhibited excellent diagnostic value for DR. miR-4687-5p expression positively correlated with clinical parameters and pro-inflammatory cytokines in DR patients. In DR cell models, miR-4687-5p overexpression inhibited cell viability, promoted apoptosis, and exacerbated inflammatory responses, whereas miR-4687-5p knockdown exerted opposite effects. Mechanistically, miR-4687-5p contributes to DR progression by negatively regulating SIRT2 to modulate cell function and inflammation.

Conclusions: miR-4687-5p is expected to become a biomarker for the early diagnosis of DR and a potential therapeutic target.